Permeability of the air-blood barrier to macromolecules is a topic of significanc in human pathology because of the increased permeability associated with respiratory distress syndrome of the adult and several forms of pulmonary edema. It is generally admitted that fluid exchange in the lung is governed by the hydraulic factors described by the Starling law. However, the alveolar epithelial and endothelial cells are endowed with billions of pinocytotic or plasmalemmal vesicles. These vesicles are unrelated to hydraulic transport mechanisms and appear to be driven only by thermal energy (brownian motion, passive diffusion). This work aims at developing and applying a reliable morphometric method for counting vesicles and defining a vesicular load of the cell surface that can be correlated with some other local property of the cell, f.i. thickness. This will yield insights into the relative significance of vesicular transport versus hydraulic transport in the lungs of laboratory animals. Subsequently, it will be investigated if changes in the amount of location of the vesicles occur in different types of experimental lung edema. Finally, it shall be investigated whether or not certain drugs, particularly those known to affect vascular permeability (f.i. histamine) or to be vasoactive (serotonin, angiotensin), influence the vesicular activity.